Complement Activation and Thromboxane Secretion by Liposome-Encapsulated Hemoglobin in Rats in Vivo: Inhibition by Soluble Complement Receptor Type 1

Janos Szebeni Department of Membrane Biochemistry, Walter Reed Army Institute of Research, Washington, DC, 20307–5100

Helmut Spielberg Department of Biochemistry and Molecular Biology, Georgetown University, Washington, DC, 20007

Richard O. Cliff Center for Biomolecular Science and Engineering, Naval Research Laboratory, Washington, DC, 20375–5000

Nabila M. Wassef Department of Membrane Biochemistry, Walter Reed Army Institute of Research, Washington, DC, 20307–5100

Alan S. Rudolph Center for Biomolecular Science and Engineering, Naval Research Laboratory, Washington, DC, 20375–5000

Carl R. Alving Department of Membrane Biochemistry, Walter Reed Army Institute of Research, Washington, DC, 20307–5100

Abstract

Intravenous administration of liposome-encapsulated hemoglobin (LEH) in rats led to an early (within 15 min) decline of hemolytic complement (C) activity in the plasma along with a significant, parallel rise in thromboxane B₂ (TXB₂) levels. The TXB₂ response was inhibited by co-administration of soluble C receptor type 1 (sCR1) with LEH, as well as by C depletion with cobra venom factor. These observations provide evidence for a causal relationship between LEH-induced C activation and TXB₂ release, and suggest that sCR1 could be useful in attenuating the acute respiratory, hematological and hemodynamic side effects of LEH described earlier in the rat.

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Complement Activation and Thromboxane Secretion by Liposome-Encapsulated Hemoglobin in Rats in Vivo: Inhibition by Soluble Complement Receptor Type 1

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Complement Activation and Thromboxane Secretion by Liposome-Encapsulated Hemoglobin in Rats in Vivo: Inhibition by Soluble Complement Receptor Type 1

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